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Acute 4526 > Test 2 week 6-9 > Flashcards

Test 2 week 6-9 Flashcards

1
Q

What do you assess when looking at A-Airway

A
  • is airway patent
  • secretions
  • mucous & vomit
  • swelling
  • tongue (LOC)
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2
Q

What are interventions to maintain Airway

A
  • open airway (head tilt chin lift & jaw thrust)
  • suction
  • oropharyngeal airway
  • nasopharygeal airway
  • HOB flat, no pillows
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3
Q

What do you assess when looking at breathing

A
  • respiratory rate, depth & rhythm
  • accessory muscle use
  • quick listen
  • SpO2
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4
Q

What are interventions for breathing

A
  • position (high fowlers/semifowlers, tripod)
  • Coached breathing - PEEP
  • Oxygen
  • Bronchodialtors
  • Bipap
  • intubation
  • ventilation - ambu bag
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5
Q

What do assess when looking at circulation

A
  • skin colour, temp, turgor
  • capilary refill
  • pulse
  • blood pressure
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6
Q

What are interventions for circulation

A
  • fluids (maybe)
  • Drugs - Epi (increase HR), norepi (constrict BV), Inotropic/anti inotropic, antiarrythmias
  • 12-lead ECG
  • IV access
  • cardioversion
    *cardiac monitor
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7
Q

What do you assess when looking at disability

A

LOC
AVPU
GCS

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8
Q

Antiarrythmic drugs

REMINDER

A

Amniodarone - tachy ventricular rhythm
Lidocaine - tachy ventricular
Adenosine - tachy atrial
Atropine - increase HR (increase symp)
BB, CA channel - decrease rate

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9
Q

What is COPD

And the two diseases seen

A

Chronic obstructive pulmonary disease
* is a respiraotry disorder largley caused by smoking and is characterized by progressive, paritally reversible airway obsturction and lung hyperventilation, systemic manifestations and increasing frequency and severeity of exacerbations
* Chronic bronchitis - chronic inflmmation of lower respriatry tract - excessive mucus secretion, cough & dyspnea
* Pulmonary emphysema - destruction of alveoli, enlargment of distal airways & breakdown of alveolar walls

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10
Q

What is the etiology of emphysema

A

Smoking & inherited alpha1-antitrypsin (anti-protease) deficiency

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11
Q

What is chronic bronchitis

A
  • large and small airway obstruction associtaed with chronic irritation from smoking & recurrent infection
  • hx of productive cough for at least 3 consecutive months in at least 2 consecutive years
  • acute exacerbations with pruluent sputum, increase in SOB, fatigue, chest congestion, fever/chills
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12
Q

What are clinical manifestations of COPD

& early, middle, late stages

A

Primary :
* cough
* sputum production
* dyspnea on exertion

Additional
* weight loss - d/t increase WOB, and interference with eating
* Chest pain - hyperinflation, loss of lung elasticity & therefore recoil
* prolonged expiratory wheeze, crackles
* Tripod positon - accessory msucle use
* Pursed lip breathing - helps prevent airway collaps
* hypoxemia, hypercapnia, cyanosis, polycythemia
* right sided heart failure form pulmonary vasocontriciton & increased PAP

Early - fatigue, exercise intolerance, cough, sputum, SOB
Middle - progressively more dyspnea with frequent infections
Late - chronic respiroatry failure, death usually 2nd to exacerbation by infection

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13
Q

How can you improve ventilation in COPD

A

**Diaphragmatic Breathing **- abdominal breathing, focuses on using diaphram instead of accessory muscle to achieve max inhalation and slow respiratory rate (tense abdomen on exhalation)
Pursed-lip breathing - prolong expiration, prevent brochiolar collapse, assist with dyspnea, - allows for effective coughing, reduce fatigue
**Postural Drainage **- promotion of airway clearance- percussion and vibration are used after the client assumes a postural drainage positon to assit in loosening the mobilized secretions

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14
Q

What can occur when giving someone with COPD too much oxygen

A

Normally, the accumulation of CO2 is a stimulate of the resp. system. however in ppl with COPD who have diminished ability to exhale properly, can have chornically higher levels of CO2 and they develop a tolerance. For these people the drive to breathe is hypoxemia - thus admisntering oxygen to patients with COPD can weaken their drive to breathe - BUT need to maintain O2 saturation

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15
Q

What are S/S of pneumonia in older adult

A

Dyspnea, chills, altered mental status (lethargy, confusion, stupor), tachypnea, hypotension, hypo/hyperthermia

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16
Q

What is Pneumonia

A

Pneumonia is an acute inflmmation of the lung parenchyma by a microbial agent - can have community-acquired or hospital-aquired pneumonia, aspiraiton pnuemonia, or opportunisitc & fungal

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17
Q

Symptoms of pneumonia & treatment

A

Sudden onset of fever, chills, cough producing purulent sputum, pleuritic chest pain, crackles
Treatment
* antibiotic treatment
* oxygen
* antipyretics (ASA, asprin, Tylenol)
* maybe analgesics
* proper nutrition

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18
Q

What are symptoms and characteristics of pleural pain

A
  • Abrupt onset
  • unilateral, localized to lower and lateral part of chest - possibly referred to shoulder
  • usually worsened with chest movement
  • tidal volume is small
  • breathing is rapid
  • reflex splinting of the chest may occur
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19
Q

What is a pleural effusion

A
  • abnormal collection of fluid in the pleural cavity - formation exceeds rate of removal
  • accumulation of fluid comes from lung, paritetal pleura, peritoneal cavity or decreased removal by lymphatics
  • fluid can be exudate, purulent, chyle, sanguinous
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20
Q

What are clinical manifestations of pleural effusion

A
  • DEPENDENT ON CAUSE
  • fever, increase WBC (if infectious)
  • fluid decreases lung expansion on affected side - decreased movement of chest wall
  • pleuritc pain
  • hypoxemia, dyspnea
  • dullness on percussion
  • absent or decreased breath sounds
  • Empyema (pocket of pus) - fever, night sweats, wt loss, cough
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21
Q

What is the Dx, Tx, & collab care for pleural effusion

A

DX & TX
* CXR, US, CT
* thoracentesis
* chest tube drainage
* rapid removal of fluid can cause hypotension, hypoxemia, pulmonary edema

Collab Care
* treat undelrying cause
* pleurodesis - prevent reaccumulation of fluid 2nd to sclerosing pleural space
* chest tubes
* antibiotics
* suppoortive - analgesia, O2, IV, antipyretic (if needed)

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22
Q

What are the 4 types of pneumothorax

A

Primary Sponatenous- usually in taller young men, 10-30 year old, ruptured bleb
Secondary spontaneous- underlying lung disease, more serious
Traumatic- penetrating or non-penetrating, may be accompanied by hemothorax
Tension - air can enter but can’t leave, area on visceral or parietal pleura as a one - way valve, life threatening, medisatinal shift, compression of great vessels (vena cava & aorta), heart and both lungs

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23
Q

Clinical manifestations of pneumothorax

A

Tachycarida, dyspnea, resp distress, chest pain, decreased air entry
Tension - severe distress, tachycardia , hypotension, tracheal shift, mediastinal shift

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24
Q

What is a hemothorax

A

Pleural effusion of blood in pleural cavity 2nd to chest injury, surgery, malignnacy, rupture of a big vessel
can have minimal (300-500cc usually reabsorbs),
moderate (500-1000cc - signs of lung compression & loss of intravascular volume, drainage & fluid replacement, maybe surgery,
large ( 1000cc +, bleeding from intercostal or mammary artery, immediate drainage, fluid replacment (possible autotransfusion) & surgery )

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25
Q

Manifestations of hemothorax

A

hypoxemia, decreased ventilation, increased effect, tachypnea, dullness, decreased air entry, S/S hypovoemia

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26
Q

Diagnosis and treatment for hemothorax

A

Diagnosis - CXR, CBC, ABGs
Treatment - Chest tube, fluid replacement, oxygen therapy
Collab - decompression, heimlich valve, chest tube, surgery, supportive - O2, IV, analgesia

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27
Q

What is pleuritis & treatment

A

Inflammation of the pleura 2nd to respiraotry infections
* sudden onset, unilateral pain
* exacerbated by inspiration
* treat underlying disease & inflammation
* NSAIDS

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28
Q

What is atelectasis & S/S

A

Incomplete expansion 2nd to airway obsturction, lung compression or increased recoil (loss of surfactant) - collapsed alveoli
S/S
* tachypnea, tachycardia, dyspnea, cyanosis, decreased expansion & absent breath sounds, m/b tracheal & mediastinal shift away from affected lung

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29
Q

What is inflammatory bowel disease

A

Characterized by chronic, recurrent inflammation of the intestinal tract - periods of remission interspersed with periods of exacerbation
No cure - treatment relies on medication to treat inflmmation and maintain remission
UC and Crohns

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30
Q

What is Ulcerative colitis

A

Diffuse inflammation beginning in the rectum and spreading up the colon, continuous (inflammation and ulceration occur in mucosa and submucosa)
Multiple absecesses develop in the intestinal glands (abscessses break through into the submucosa, leaving ulcerations)

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31
Q

Pathology of Crohns

A
  • Inflammation involves all layers of the bowel wall
  • skip lesions - segments of normal bowel occurring between diseased portions
  • ulcerations are deep and longitudinal, & penetrate between islands of inflamed edematous mucosa, causing the classic cobblestone appearance
  • narrowing of the lumen with stricture development - may cause bowel obstruction
  • microscopic leaks can allow bowel contents into peritoneal cavity
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32
Q

What are the clinical manifestations of crohns

A
  • exacerbation & remission
  • intermittent diarrhea
  • colicky pain (RLQ)
  • weight loss
  • fluid & electrolyte disorders
  • malaise
  • low grade fever
  • depends on the anatomic site of involvment, extent of the disease process, nonbloody diarrhea, malabsoprtion, nutirontal deficiencies
  • **non bloody dairrhea & colicky abdominal pain **
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33
Q

Clinical manifestations of Colitis

A
  • relpasing periods of diarrhea, bloody, mucousy stools
  • mild abdmonial cramping, fecal incontinence, noctural diarrhea, anorexia, weakness, fatigue
  • chronic disorder with mild-to-severe acute exacerbation, unpredictable intervals, nonspecifc complaints (abdominal pain, weight loss, fever) tensemus & rectal bleeding
  • bloody diarrhea and abdominal pain
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34
Q

Complications of IBD

A
  • obstruction & fistulas malabsorption, dehydration, fluid & electrolyte imbalances, anemia
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35
Q

How do you diagnose IBD

A
  • HX & physical exam
  • sigmoidoscopy
  • colonoscopy
  • biopsy
  • barium enema
  • stool specimens
  • ESR
  • electrolytes, CBC
  • invasive - scopes - usually not in presence of active disease
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36
Q

Treatment for Crohns & goals of care

A

Crohns
* DRUGS: corticosteriods, immunosuppressants, aminosalicylates, antidiarrheals, anti-TNF agents (prednisone, biologic agents, antibacterials)
* lifestyle - stress reduction, decreased physical activity, vitamins, eliminating high fibre foods, dairy, spice, fat, coffee - TPN for bowel rest during acute excerbations
* Surgery - last resort - 75% will require surgery, it produces remission but high recurrence rate, ileostomy
* GOALS of treatment : rest the bowel, control inflammation, combat infection, correct malnutrition, alleviate stress, symptomatic relief, improve quality of life

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37
Q

Treatment of Colitis

A

Colitis
* Drugs : corticosteriods, immunosuppressants, aminosalicylates, antidiarrheals, anti-TNF agents (prednisone, biologic agents, antibacterials)
* Diet - low residue diet, drink suppments, TPN if required
* Surgery - surgical therapy - total colectomy
* GOALs of treatment - rest the bowel, control inflammation, combat infection, correct malnutrition, alleviate stress, symptomatic relief, improve quality of life

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38
Q

Teaching for IBD (colitis/crohns)

A
  • importance of rest and diet management
  • perianal care
  • action and side effects of drugs
  • symptoms of recurrence
  • when to seek medical care
  • use of diversional activites to reduce stress
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39
Q

What is the relationship between potassium and diabetes

A
  • insulin increase the permeability of many cells to potassium, magnesium and phosphate ions
  • the effect on potassium is clinically important - insulin activates sodium-potassium pump in many cells, causing a flux of potassium into cells
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40
Q

Acute complications of diabetes mellitus

A
  • diabetic ketoacidosis
  • hyperglycemic hyperosmolar nonketotic syndrome
  • hypoglycemia
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41
Q

Chronic complications of diabetes mellitus

A
  • macrovascular disease: CAD, CVD, PVD
  • Microvascular disease : kidneys & eye
  • neuropathic : involving nerves, depends on what nerve is involved
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42
Q

what are charactersitics & manifestations of DKA

A

only occurs in type 1 diabetes
* hyperglycemia
* ketonuria
* acidosis - kussmaul resp, abdominal tenderness, N/V, altered LOA
* dehydration - tachycardia, dry mm, poor turgor, poor perfusion, hypotension, altered LOA, orthostatic drop
* ketosis - acetone odor to breath
* hyperosmoality - altered LOA, polyuria, polydipsia

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43
Q

What is pathology of DKA

A
  • combination of insulin deficiency & metabolic stress
  • insulin deficiency - new onset, omitted dose, insufficient dose to compensate for illness stress
  • Metabolic stress - glucagon, cortisol, epinephrine (released 2nd to illness/deficiency) - increase glucose production, impair peripheral uptake, increase proteolysis & lipolysis
  • lipolysis, proteolysis, ketosis - met. acidosis
  • hyperglycemia - hyperosmolaity, osmotic diuresis, dehydration, urinary electrolyte loss
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44
Q

Lab values in DKA

A
  • increased glucose
  • ketonuria, glycosuria
  • sodium - prolonged hyperglycemia can depress sodium but dehydration can increase - evlaute after fluid resusitation
  • potassium - initally appears increased but actual body potassium is depleted
  • bicarbonate (HCo3) - <4 severe, 4-14 moderate, 12-20 mild
  • CO2 10-20
  • ph - <7.3
  • CBC - increased wbc 2nd to stress or infection
  • serum ketones - positive
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45
Q

How do you treat DKA

A

IV Insulin & fluids (note insulin will decrease serum potassium, & no rapid fluid resuscitation) - IV insulin only way to reverse DKA
* ensure patent airway, O2 as needed
* IV NS until BP stable - output 30-60ml/hr
* insulin infusion - for aciodsis 0.1U/kg/hr (bc decreases lactic acid prodcution, increases glucose availability)
* Switch to D5W when Blood glucose apporach 14mmol/L
* after inital treatment correct fluids loss, plus K+

46
Q

What are the classes of hypoglycemia & risk factors

A

Mild - pale, sweaty, tachyacrdia, usually self-treat
Moderate - impaired concentration, slurred speech, H/A blurred vision, awkward gait
severe - may be incapacitated, uncooperative seizure
Risk factors - >50% nocturnal, too much insulin or oral medication, not compensating (wt loss, menses, execrise, ETOH, decreased caloric intake)

47
Q

What is treatment for hypoglycemia

A

Mild to moderate - 15g of glucose as concentrated carbohydrate, retest BG in 15mins & repeat if BG <4mmol/L (ex. glucose tablets, sugar, juice, lifesaver, honey)
Severe - Img of glucagon sc or IM, 20-50ml D50W over 1-3min, conscious pt 20g carbohydrate, check BS 15 min later if OK recheck in 2-3 hours

48
Q

What is PACU

A

Post anesthesia Care Unit - patient is coming out of anesthesia lots of concerns with resp function & LOC
considered critical care area as patients are unstable, after transfer there is indepth assessment performed and intiation of postoperative order
* early ambulation for muscle tone, gastrointestinal and urinary function, stimulation of criculation, and normal respriatry function

49
Q

Summary of effects on body systesm post surgery

Neuro, resp., urinary, cardio., gastro, integumentary, fluid & lyte

A
50
Q

What is part of nursing assessment in PREop

A

goals, anxiety, fear & hope, health hx, current medications, ROS (review of systems) physical exam

51
Q

What is part of client interview PREOP

A
  • check documented informaiton prior to interview
  • occurs in advance or on day of surgery
  • PURPOSE - obtain health infromation, determine expectations, provide and clarify infromaiton on procedure, assess emotional state and readiness, begin some post-op teaching
  • Overall goal - idenitfy risk facotrs, plan care to ensure client safety
  • Note - scheduled surgery process is much smoother compared to emergency
52
Q

What are goals of the preop nursing assessment

A
  • determine psychological status to reinforce coping
  • psycholgical factors of procedure contrubting to risks
  • identify cultural and ethnic factors that may affect surgical experience
  • determine receipt of adequate infromation from surgeon in order to sign infromed consent
  • identify any psychosocial needs of the client
  • establish baseline data
  • idenitfy meidcations and herbs taken that may affect surgical outcome
  • identify, document, and communciate results of labroatory/diagnostic test
  • surgeons obligation is informed consent
53
Q

What are infleuncing factors part of preop assessment

A

age, past experience, current health, socioecnomic status

54
Q

How does anxiety affect preop assessment or surgery

A
  • anxiety can impair cognition, decision making & coping
  • anxiety may arise from conflict with interventions (i.e. blood transfusions) & religious beleifs
  • lack of knowledge - information lessens anxiety
  • unrealistic expectations
  • identify beleifs in nonjudmgental way and discuss with surgeon and operative staff
55
Q

What can people fear when it comes to surgery

A
  • death or disability (may prompt postponement, influence outcome)
  • pain - consult APS, reassure drugs will be available
  • mutiliation/alteration in body image (be nonjudgmental)
  • anesthisa - assess malignat hyperhtermia risk
  • disruption of life functioning - range form fear of permanent disbaility to temporary loss, family & financial concerns, consultations (CCAC & social work b4 surgery)
  • lack of control
56
Q

What is important about hope with surgery

A
  • hope is strongest positive coping mechanism - never deny or minmize, assess and support
  • do not need to agree wiht them but also do not need to decline
57
Q

What is gathered with health history in preop assesment

A
  • medical conditions
  • previous surgeries and problems (c-section counts*)
  • menstrual/obstetric hx
  • familial diseases
  • reactions/problems to anesthesia (client or family)
  • analgeisa/pain conversation
58
Q

What is gathered when looking at current medications in preop assessment

A
  • prescription and OTC
  • herbs
  • vitamins
  • recreational - drugs, alcohol, tobacco
  • need to ask abt recreational, often they will not come out and say it, or do not think they are alcoholic but with the amount they drink need to be aware of withdrawl and damage to liver with metabolism of medication
  • smoking alters defense mechanism - build up, less movement with anesthesia
59
Q

What is included with ROS Cardio PREOP

A
  • Report - problems for effective monitoring, use of cardiac drugs, presence of pacemaker/MI
  • vitals preop for baseline
  • bleeding/clotting time
  • lab results
  • possible prophylactic antibiotics
60
Q

What is included with ROS Respiraotry in PREOP

A
  • inquire about recent airway infections - procedure should be canceled if risk for laryngo/bronchospams or decreased SaO2
  • hx of dyspnea, coughing, hemoptysis
  • COPD/ asthma - high risk for atelactasis & hypoxemia
  • smokers should be encouraged to quit 6 weeks b4 procedure - decrease risk of complications
61
Q

What is included in ROS Neuro PREOP assessment

A
  • evaluation of neurolgical functionning - vision/hearing loss
  • cogntive function - postop delirium can be labeled as dementia but it is not - can occur with dehydration, hypothermia, and medications
  • if there are declines in cogntive funciton that are not permanent need to correct b4 surgery ex lyte imbalances
62
Q

What is included with ROS Renal PREOP assessment

A
  • HX of urinary or renal disorders
  • renal dysfunction contributes to - fluid/lyte imbalance, coagulaopthies, impaired wound healing, altered response to drugs and elimination
  • renal function tests
  • problems voiding
63
Q

What is included in ROS heaptic PREOP assessment

A

Presence of liver disease - jaundice, hepatitis, alcohol abuse
Liver function tests : ALT, AST, ALP, bilirubin

64
Q

What is included in ROS integumentary PREOP assessment

A
  • hx of skin and musculoskeletal problems - extra padding during procedure, affest postop bleeding
  • hx of pressure ulcers
65
Q

What is included in ROS musculoskeletal PREOP assessment

A
  • idenitfy joints affected with arthritis
  • mobility restrictions may affect positiong and ambulation
  • bring mobility aids to surgery
  • report problems affecting neck or lumbar spine - can affect airway managmnet and anaesthesia delivery
  • want them mobile ASAP post-op
66
Q

what is included in ROS endocrine PREOP assessment

A

Clients with diabetes are at risk for
* hypo/hyperglycemia
* ketosis
* cardiovascular alterations
* delayed wound healing
* infection
* cap. blood glucose tests- baseline

clients with thyroid dysfunction
* hyper/hypothyroidism - risk due to altered metabolic rate
* verify with anesthesiologist about giving medications

67
Q

What is included with ROS Immune system preop assessment

A
  • clients with hx of compromised immune system or use immunosuppressive drugs can have - delayed wound healing or increased risk for infection

*

68
Q

What is included with ROS fluid & lyte preop assessment

A
  • vomiting, diarrhea, or difficulty swallowing can cause imbalance
  • identify drugs that alter status - diuretics
  • evaluate serum lyte levels
  • NPO status - may require additional fluids and lyts prior to surgery if dehydration occurs
69
Q

What is included in ROS nutriontal status preop assessment

A

obesity
* stresses caridac and pulmonary systems
* increased risk of wound dehiscence and infection
* slower recovery from anaesthesia
* slower wound healing

Extra padding to prevent pressure ulcer
identify dietary habits that may affect recovery (caffeine)
*when cutting through all the layers of skin need proper nutrion to build them back up

70
Q

What is included with preop teaching

A
  • explain to client what to expect, how to participate (increases client satisfaction, reduces fear, anxiety, stress, pain)
  • limited time - so address highest priority - focus on client concerns and provide written material
  • provide edcuation several days before surgery - determine what teaching still necessary, anxiety/fear can hinder learning
  • must be documented and reported to postop nurses
  • teach deep breathing, coughing, moving postop
  • inform if tubes, drainage, monitoring or special equipment will be used post op
  • basic info - time/place, fluid/food restriction, need for enema or other prep, need for shower
71
Q

What is included in legal preparation before surgery (preop)

A
  • informed consent - must include adequate disclosure, understanding, comprehension, voluntary - surgeon is responsible for getting conset nurse can be witness signature
  • blood transfusion
  • advance directives
  • POA
  • all required forms are signed and in chart (esp with minor)
  • medical emergency can override need for consent
72
Q

What is done on day of surgery

A
  • final preop teaching
  • assessment Head to toe
  • verify consent
  • labs
  • hx and physical examination
  • baseline vitals
  • consualtion records
  • nurses notes
  • chart review
  • surgical site marked - ID band, allergy band, VS, valubles
  • client - no cosmetics, dark nail polish,
  • void before surgery to avoid accidental involuntary elimination under anestheisa or urinary retention (often foley catheter but still important)
73
Q

What are 7 Preop medication classes/types

A
  • benzodiazepine and barbiturates for sedation and anti-anxiety
  • anticholinergics - reduce secretions
  • narcotics - decrease intraoperative anaesthetic requiremnts & pain
  • antiemetics - decrease post op nausea and vomiting
  • antibiotics (prophylaxis)
  • eyedrops (eyes may dry out)
  • routine prescription drugs
74
Q

Age related considerations for surgery

A

Older adult - greater risk with anestheisa, surgery, postop complications

75
Q

What are potential alteration in respriatry function POSTOP & who at risk

A
  • obstruction - blockage from tongue LOC, supine, sleepy, laryngospams, retained secretions, laryngeal edema
  • hypoxemia - agitation, hypertenison/hypotension, tachy/brady. ABG to confirm
  • hypoventilation - depression of central respiratory drive/ poor muslce tone, causes - anesthesia, narcotic analgesia
  • RISK - general anesthesia, are older, smoke heavily, with lung disease, who are obese, undergoing thoracic, airway or abdominal surgery
76
Q

Conditions that can occur POST op in resp system

A

* atelectasis - from postop hypoxemia, bronchial obsutrction from retained secretion or decrease excursion
* pulmonary edema - caused by accumulation of fluids in alveoli, fluid overload, left ventricular failure, prolonged airway obstruction, sepsis, aspiration — S/S hypoxemia, crackles
* aspiration of gastric contents - clients at risk can be given histamine H2 receptor antagonist before induction of anesthesia to prevent HCI secretion - usually minimized bc NPO but can give PPI
* **Bronchospams **- results from increase in bronchial smooth muscle tone, with resultant closure of small airways - edema develops causing secretions to build up, S/S - wheeze, dyspnea, accessory muscle use, hypoxemia, tachypnea

77
Q

Nursing care post op for resp system

A
  • assess temp, oximetry, resp rate, pattern, breath sounds (temp norm elevated post op
  • airway patency - chest symmetry
  • sputum

teach deeo breathing & coughing - prevents alveolar collapse, move secretions to larger airway passages, deep breathing 10 times every hour while awake, incentive spirometer, splinting abdominal incision

78
Q

Potential alterations in Cardiac function postop

A

Note - postop - often have positive fluid balance however there is normal & excessive (stress response - fluid retention)
PACU
* hypotension - bc unreplaced fluid & blood loss, dysrhythmias, low systemic vascular resistance, incorect cuff
* hypertension - results from sympathetic stimulation form pain, anxiety, bladder distension or resp compromise, hypothermia, pre-exisiting, revascularaization during surgery
* dysrhythmias - often from identifiable cause - hypokalemia, hypoxemia, hypercarbia, alterations in acid-base status, circulatory instability, preexisiting

Clinical unit
* hypokalemia - can result from urinary or gatro losses, affects contractiltiy of heart
* stress resonse - increased clotting facotrs, DVT and PE
* syncope - can indicate decreased CO, fluid deficit, deficit in cerebral perfusion, postural hypotentions on ambulation, common with immobile & elderly

79
Q

Nursing care for cardiac post-op

A
  • frequent VS
  • apical, radial pulse
  • skin color, temp, turgor
  • NOTIFY anaesthesiologst if - systolic < 90, or >160, pulse < 60, or >120, pulse pressure narrow, irregualr cardiac rhythm develops, significant variations
  • I & Os, lab findings, mouth care, leg exercises
  • elastic stockings or compressive devices
  • unfractured or LMWH
  • ambulation - slowly, monitor pulse, assess for pre-syncope
80
Q

Potential alterations in neurological function post op

A
  • emergence delirium (or violent emergence) - can induce restlessness, agitation, disorientation, thrashing, shouting. Caused by anesthetic agent, hypoxia, bladder distension, pain, electrolyte abnormalities, anxiety
  • delayed awakening - commonly caused by prolonged drug action - can be poor liver or kidney metabolism
81
Q

nursing care post op neuro

A
  • LOC - AVPU, GCS
  • orientation, follow commands, PERRLA, sensory/motor status
  • PACU - attention on resp function, sedation (controlling agitation) side rials up, secure IV, aritifical airways, monitor
  • Clinical - some alterations related to pain medication, lack of sleep or sensory overload, complete CNS, those getting pain meds ensure alert/oriented x3, assessing sensation in those with spinal/epidural anesthetic
82
Q

nursing care for pain postop & treatment

ways of adminstering (PCA, epidural)

A

PACU - may be diffciult to assess, often still sedated, behavioural cues and increased pulse
Clinical - charactersitics, location, measure before and after treatment, new pain can be complication
Post op- first 48 hours narcotic analgesic to relieve moderate - severe pain, after non-narcotic
before giving analgesic nature of pain, chest/leg can be complication, gas pain can be worsened by narcotic
PCA - pt can give themsleves boluses (some have background infusion)
Epidural - delivers directly to opiod receptors in spincal cord, can decrease resp. symptoms of narcotics, anesthetic in spinal cord can cause resp problems.

83
Q

Potenital Alterations in Temperature postop

A

**PACU ** - hypothermia - loss of heat to cold or form body organs exposed to air (risk - age, debility, intoxication, prolonged anesthetic adminstrations) - complications (compromised immue function, pain, increased bleeding, MI, delayed drug metabolism)
**Clinical ** - temp elevation - mild elevation (38 in first 48 hours ) is normal, stress response, after 48 hrs moderate to marked elevation could mean infection (wound infection, fever spiking in afternoon, tender, warm, red, purulent- if intermittent high with shaking chills & diaphoresis indicates sepsis ) - rule out pneumonia & Cdiff

84
Q

Nurisng care temp alterations postop

A
  • VS (possibly rectal temp bc most accurate)
  • color & temp of skin
  • PACU - rewarming, heated blanket, etc, monitor temp q15min when using external warming device, o2 therapy - monitor for malignant hyperthermia
  • Clinical - measure temp q4hr first 48hrs postop, assess wound and IV site, airway clearance, chest x-ray/culture if infection suspected, anti-pyretic over 39.4
85
Q

potential gastrointestinal problems postop & causes

A
  • N/V - esp after abdominal surgery - caused by anesthetic, opiods, delayed gastric emptying, slowed peristalsis, resumption of oral intake too soon postop - may have swallowed air & secretions can accumulate - distension & gas pain, releived by exercise/walking
  • Paralytic ileus - small bowel obstruction when peristalsis stops, produces severe N/V, noticed on clinical unit, may be neuro or muscular impairment, assess for distension & absence of bowel sounds, if passing gas - do not have
  • hiccups (singultus) - spasm of diaphragm by irritation of phrenic nerve - direct (gastric distension, intestinal obstruction, intra abdominla bleeding, subphrenic abscess) indirect ( acid-base & electrolyte imbalance), reflex irritation - drinking hot / cold liquid or presence of NG tube
86
Q

Nursing care postop for gastrointestinal problems

A
  • N/V - document vomitus
  • paralytic ileus - auscultate
  • antiemtic drug
  • suction at bedside
  • upright position
  • slow, deep breathing
  • resume intake upon return of gag reflec
  • for abdominal surgery NPO until bowel sounds returm (IV/NG decompression)
  • clear liquids - advance as tolerated
  • mouth care when NPO
  • ealry & frequent ambulation to prevent abdominal distension & relief of gas pain
87
Q

Potential alteration in urinary function postop, assessment & treatment

A
  • low urinary output expected in first 24 hours (increase aldosterone, ADH from stress, fluid losses during surgery, anestheisa depresses nervous system) opiods use can also interfere
  • examine urine colour, amount, consistency, & odor
  • if in-dwelling catheter assess - 30 ml/hr output
  • or void 200ml following surgery
  • use running water, drinking water, pouring water over perineum, ambulation, bedisde commode
  • may need to reestablish foley catheter
88
Q

potential alterations of the integument post-op & what causes them

A
  • adequate nutrition - need protein, can have nutritional deficits from chronic disease
  • impaired wound healing - in older adult & those with chronic disease
  • accumulation of fluid in wound can impair healing & predispose to infection (jackson-pratt drain, closed system)
  • wound infection - can be from flora in environment on skin, oral or intestinal flora
  • increase incidence of wound spesis in those who are - malnourished, immunosuppressed, older adult, proonged hospital stay
  • wound infection evident 3rd-5th day post op (redness, edema, pain, tenderness, leukocytosis, fever)
89
Q

What is included in nursing assessment of surgical wound

A
  • type of wound & expected drainage needs to be known
  • drainage should go from sanguineous, serosanguineous to serous with decreased output
  • would dehiscence - may get sudden brown, pink or clear discharge
  • note type, amount, color, consistency and odor of drainage
  • notify surgeon of excess or abnormal drainage & significant changes in vital signs
  • clean gloves & sterile technique
90
Q

Potential alterations in psychological function postop

A
  • anxiety & depression - do they have hx, may lack knowledge, resources
  • confusion & delirium - from psychological & physiological sources - fluid & electrolyte imbalance, hypoxemia, drug effects, sleep depreivation, sensory alteration/overload - delirium tremors (DTs) from alcohol withdrawl
  • provide adequate support - listen and talk with client, discuss expectations of activtiy and assistance, include in discharge planning, report unusal behavior
  • recognize alcohol withdrawl syndrome
91
Q

what is included in clinical unit discharge postop

A
  • pt gradually assumes greater responsibility for self-care during post-op period
    pt should know
  • care of wound site, dressings, bathing
  • action, side effects, when and how to take medications
  • activties allowed/prohibited
  • dietrary restrictions/modifications
  • symptoms to report
  • intructions for follow-up care
  • answer questions concerns
  • follow-up call/visit - work discharge planner, can be done with CCAC
92
Q

What is chronic stable angina

A
  • reversible (temporary) myocardial ischemia = angina (chest pain) - when oxygen demand is more then oxygen supply
  • primary reaons for insufficient blood flow is narrowing of coronary arteries by atherosclerosis - for ishcemia to occur artery usually 75% or more stenosed
  • pain usually lasts 3-5 minutes - subsides whem the precipitating factor is releived ex stop walking and sit, ECG shows ST segment depression
93
Q

What are precipitating factors and diagnostic studies for chronic stable angina

A

Precipitating
* physical exertion, temperature extremes
* strong emotions
* heavy meal, tobacco use, sexual activity
* circadian rhythm - early morning after waking

Diagnostic
* health hx & physical examination
* laboratory studies
* 12-lead ECG
* chest x-ray
* echocardiogram
* excerise stress test

94
Q

What are the 4 types of angina

silent, nocturnal, decubitus, prinzmetals angina

A
  • Silent ischemia - asymptomatic, assoicated with diabetes mellitus
  • **Nocturnal angina **- occurs only at night but not necessarily during sleep
  • angina decubitus - chest pain that occurs while lying down, relieved by standing or sitting
  • ** prinzmetals (variant) angina **- occurs at rest usually in response to spasms of major coronary artery, seen in clients with a hx of migraine headaches or raynauds, may be relieved by moderate exercise, there is ST elevation but after spams is over ST normal
95
Q

What drugs are used to treat chronic stable angina

A
  • give O2 or decrease O2 demand
  • short acting nitrates - sublingual nitro
  • long acting nitrates - isordil
  • B-adrenergic blockers or calcium channel blockers
  • angiotension-converting enzyme inhibitors
  • maybe antiplatelet therapy & lipid-lowering drugs
  • manging risk factors of CAD
  • possible PCI or CABG
96
Q

What is ACS

A

Acute coronary syndrome
* when ischemia is prolonged and not immediately reversible, acute coronary syndrome develops
* deterioration of a once stable plaque that stimulates platelet aggregation and local vasocontrition with thrombus formation
Results in
* parital occlusion of coronary artery - UA or NSTEMI
* total occulsion of coronary artery STEMI

97
Q

How do you treat unstable angina

A
  • it is unpredictable and represents medical emergency
  • acute intensive drug therapy
  • nitroglycerin
  • low-molecualr weight heparin
  • clopidogrel (plavix) - antiplatelet
  • glycoprotein llb/llla inhibitors
  • PCI
98
Q

What is a myocardial infarction

A
  • result of sustained ischemia (>20minutes), causing irreversible myocardial cell death (necrosis)
  • necrosis of entire thickness of myocaridum tales 4-6 hours
  • the degree of altered function depends on the area of the heart involved and the size of the infarct
  • contractile function of the heart is disrupted in areas of myocardial necrosis
  • most MI involve the left ventricle
99
Q

what are the clinical manifestations of ACS

A
  • **pain ** - total occlusion you will get anaerobic metabolism and lactic acid accumulation - severe immoblizing chest pain not releived by nitro, heaviness, constriction, burning, pressure, curhsing
  • pain location - substernal, retrosternal, epigastric areas, pain can radiate to arm and jaw
  • Sympathetic nervous system stimulation from catecholamines released from ischemic myocardial cell - release glycogen, diaphroesis, vasocontriciton of peripheural - skin - ashen, clammy, cool to touch
  • initally increase HR and BP - then decreased BP (bc decreased CO) - crackles, jugular vein distension, heaptic engorgemnt & peripheral edema
  • abnormal heart sounds - S3, S4, holosystolic murmur
  • Nausea and vomiting - result from stimulation of the vomiting centre by the severe pain
  • fever - increases during first 24 hours and may persist for 1 week
  • systemic manifestation of the inflmmaotry process caused by cell death
100
Q

What is the healing process post ACS

A
  • within 24 hours leukocytes infiltrate the area of cell death
  • enzymes are released form the dead cardiac cells
  • proteolytic enzymes of neutrophils and macrphages remove all necrotic tissue by second/third day
  • development of collateral circulation improves areas of poor perfusion
  • necortic zone identifed by ECG changes & nuclear scans
  • 10-14 days after MI, scar tissue is still weak and vulnerable
  • by 6 weeks after MI, scar tissue has repalced necortic tissue - area is healed but less compliant
  • ventricular remodeling - in an attempt to compensate for the infarcted muslce, the normal myocaridum will hypertorphy and dialte - can lead to development of late heart failure
101
Q

What are complications of ACS

A
  • Dysrhythmias
  • heart failure
  • cardiogenic shock - occurs when inadequate oxygen and nutrients are supplied to the tissues becasue of severe LV failure
  • papillary muslce dysfunction - causes mitral valve regurgitation and aggravates an already compromised LV
  • ventricular aneurysm - results when the infarcted myocardium wall becomes thinned and bulges out during contraction
  • acute pericarditis - inflmmation of pericardium - chest pain different form MI, may result in cardaic compression, decreased LV filling and emptying, heart failure - friction rub
  • dressler syndrome - characterized by pericarditis with effusion and fever that develop 4-6 weeks after MI , arthralgia
102
Q

what are two main treatments for MI

A
  • emergent PCI - treatment of choice for confirmed MI, balloon angioplasty + drug-eluting stent
  • fibrinolytic therapy - major complication is bleeding, resuce PCI if thrombolysis fails - does not dissolve clots only breaks apart
103
Q

Diagnostic studies MI

A

detailed hx, 12-lead ECG, ST segment elevation for STEMI
serum caridac markers (troponin, CK-MB, myoglobin)
coronary angiography
excersise stress testing, echocardiogram

104
Q

Drug therapy in MI

A
  • IV nitroglycerin
  • morphine sulphate
  • B-adrenergic blockers
  • angiotensin-converting enzyme inhibitors
  • antidysrhtyhmia drugs
  • cholesterol-lowering drugs
  • stool softners
105
Q

Nursing Care for coronary revascularization

A
  • ICU for first 24-36 hours
  • pulmonary artery catheter for measuring CO, & hemodynamic parameters, intraarterial line for BP, chest tubes, continuous ECG, endotracheal tube (extubation within 12 hours)
  • epicardial pacing wires for emergency pacing
  • catheter
  • NG tube for gastric decompression
106
Q

What are complicatins of CABG

A
  • bleeding and anemia form damage to RBCs and platelet
  • fluid & electrolyte imbalance
  • hypothermia as blood cooled as it passes through bypass machine
  • nursing care focsued on assesseing for bleeding, monitroing fluid status, replacing electrolytes & restoring temperature
107
Q

GENERAL - diagnostic with chest pain

A
108
Q

general collab care for ACS

A
109
Q

Collab care unstable angina & NSTEMI

A
110
Q

collab care STEMI

A
111
Q

Emergency management

not question - table from textbook

A
112
Q

what is normal pH, PaO2, SaO2, PaCO2, HCO3

A

ph - 7.35-7.45
PO2 80-100mmHg
SaO2 -95% above
PaCO2 - 35-45
HCO3 - 22-26 mmol/L

Acute 4526 (4 decks)

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